Immunohistochemical distribution of glucagon-like peptide 1 in the digestive system of different aquatic vertebrates.

The distribution of glucagon-like peptide 1 (GLP-1)-positive cells in digestive tracts and pancreases of aquatic vertebrates was investigated by immunohistochemical staining method. The results suggested that GLP-1-positive cells were distributed in the columnar mucous epithelium and tubular glands of lamina propria in the digestive system. However, GLP-1-positive cells were also found in subepithelial lamina propria of the mucosae and muscularis in each segment of the digestive tract of Rana nigromaculata. The distribution densities of these cells reached peaks in the stomachs, and the middle or end segments of small intestines of Chinese softshell turtle, Bufo gargarizans, R. nigromaculata and catfish, and there was the third distribution density peak in the rectum of catfish. The total amount or overall density of GLP-1-positive cells varied a lot in the digestive tracts of different animal species. The distribution density was relatively low in the digestive tract of chub and reached the maximum in the digestive tracts of snakehead and catfish, but no GLP-1-positive cells were found in the digestive tract of bighead carp. GLP-1-positive cells were densely distributed in the pancreases of Chinese softshell turtle, B. gargarizans and R. nigromaculata. These cells spread over the superficial layers of islets or scattered in exocrine pancreas in the pancreas of B. gargarizans, spread in the endocrine cells or scattered in the pancreas of Chinese softshell turtle, scattered in the pancreas of R. nigromaculata and distributed in the superficial layers of islets in the pancreas of catfish.

The Regulatory Effects of Lateral Hypothalamus Area GABAB Receptor on Gastric Ischemia-Reperfusion Injury in Rats.

HIGHLIGHTS The aim of the research was to determine the functional effects and molecular mechanisms of GABAB receptor on ischemia reperfusion-induced gastric injury in rats.The lateral hypothalamus area GABAB receptor attenuated the ischemia reperfusion-induced gastric injury by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the brain.This work would provide a new therapeutic strategy for acute gastric injury. Gastric ischemia-reperfusion (GI-R) injury progression is largely associated with excessive activation of the greater splanchnic nerve (GSN). This study aims to investigate the protective effects of GABAB receptor (GABABR) in the lateral hypothalamic area (LHA) on GI-R injury. A model of GI-R injury was established by clamping the celiac artery for 30 min and then reperfusion for 1 h. The coordinate of FN and LHA was identified in Stereotaxic Coordinates and then the L-Glu was microinjected into FN, GABAB receptor agonist baclofen, or GABAB receptor antagonist CGP35348 was microinjected into the LHA, finally the GI-R model was prepared. The expression of GABABR, P-GABABR, NOX2, NOX4, and SOD in the LHA was detected by western blot, PCR, and RT-PCR. The expression of IL-1ß, NOX2, and NXO4 in gastric mucosa was detected by western blot. We found that microinjection of L-Glu into the FN or GABAB receptor agonist (baclofen) into the LHA attenuated GI-R injury. Pretreatment with GABAB receptor antagonist CGP35348 reversed the protective effects of FN stimulation or baclofen into the LHA. Microinjection of baclofen into the LHA obviously reduced the expression of inflammatory factor IL-1ß, NOX2, and NOX4 in the gastric mucosa. Conclusion: The protective effects of microinjection of GABABR agonist into LHA on GI-R injury in rats could be mediated by up-regulating the production of GABA, GABABR, and down-regulating P-GABABR in the LHA.

Abscisic acid treatment alleviates cadmium toxicity in purple flowering stalk (Brassica campestris L. ssp. chinensis var. purpurea Hort.) seedlings.

The aim of this research was to investigate how exogenous abscisic acid (ABA) alleviates cadmium (Cd) toxicity in purple flowering stalk (Brassica campestris L. ssp. chinensis) and evaluate whether it could be a potential choice for phytoremediation. Purple flowering stalk seedlings were cultivated in a hydroponic system with Cd at various concentrations (0-100 µmol L-1) as controls and Cd plus ABA as the treatment in the growth media. The soluble proteins, chlorophyll contents and the activity of the antioxidant enzyme system were determined by previously established biochemical methods. The contents of soluble protein and chlorophyll, and the activities of superoxide dismutase (SOD, EC 1. 15.1.1), peroxidase (POD, EC 1.11.1.7), ascorbic peroxidase (APX, EC 1.11.1.11), glutathione reductase (GR, EC 1.8.1.7) and superoxide anion (O2·-) increased with the increase of external Cd concentrations, and then decreased in both Cd and Cd+ABA treatments, with higher activities of enzymes but lower level of O2·- in Cd+ABA than those in Cdonly treatments. It indicated that a stress adaptation mechanism was employed at lower Cd concentrations. The contents of malondialdehyde (MDA) and hydrogen peroxide (H2O2), increased with the increase of Cd concentrations in the growth medium, with the highest levels in the treatment of 100 µmol L-1 Cd with lower levels in respective Cd+ABAtreatments than the Cd only treatmetns. Plants treated with 100 µmol L-1 Cd plus ABA showed a 60% decrease in Cd content in the leaves but a 259% increase in Cd content in the roots. In summary, exogenous ABA might alleviate Cd toxicity in purple flowering stalk mainly by reducing the reactive oxygen species (ROS) though activing the antioxidant enzyme system and accumulating more Cd in roots.

GABA(A) receptor overexpression in the lateral hypothalamic area attenuates gastric ischemia­reperfusion injury in rats.

Excessive activation of the greater splanchnic nerve (GSN) has previously been determined to contribute to the progression of gastric ischemia­reperfusion (GI­R) injury. The present study was designed to estimate the protective effects of GABAA receptor (GABA(A)R) overexpression in the lateral hypothalamic area (LHA) against GI­R injury. The GI­R injury model was induced in rats by clamping the celiac artery for 30 min and then reperfusing for 1 h. Microinjection of recombinant adenoviral vectors overexpressing GABA(A)R (Ad­GABA(A)R) or control adenoviral vectors (Ad­Con) into the LHA was conducted in GI­R and normal control rats. Significant protective effects were observed on day 2 after Ad­GABA(A)R treatment in the GI­R injury rats. Ad­GABA(A)R treatment reduced plasma norepinephrine levels, plasma angiotensin II levels and peripheral GSN activity, but increased the gastric mucosal blood flow, as compared with Ad­Con treatment. These results indicate that adenoviral vector­induced GABA(A)R overexpression in the LHA blunts GSN activity and subsequently alleviates the effects of gastric injury in GI­R rats.